JUN and glomerulosclerosis: JUN proteins can form homodimers or heterodimers in combination with FOS proteins, which are involved in forming Activator Protein 1 (AP-1).[20] AP-1 participates in the progression of multiple pathological processes, including fibrosis and inflammation.[21] Activation of AP-1 may lead to glomerulosclerosis, interstitial fibrosis, and inflammation, which are essential causes of kidney injury.[22] As one of the 3 MAPK signaling pathways, c-Jun amino-terminal kinase (JNK) can transmit extracellular signals to regulate cell proliferation, differentiation, and apoptosis.